Many patients with anginal chest pain and normal epicardial coronary arteries show abnormal coronary flow response to electrical pacing, the vasoconstrictor, ergonovine and the vasodilator, dipyridamole. These stimuli, in fact, often reproduce their chest pain. The studies eliciting these data suggest these patients have dysregulation of vascular smooth muscle tone, and, in particular, decreased vasodilator reserve. To examine if these phenomena represent a more generalized abnormality of vascular smooth muscle function, we studied another vascular bed by studying blood flow to skeletal muscle in the forearm. We used the non-invasive technique of strain-gauge plethysmography and studied vasodilator capacity by subjecting the forearm to ischemia (an upper arm cuff inflated to supra- systolic pressures) of increased lengths of duration. Compared to a control population of comparable age and sex, the patients with microvascular angina had blunted peak flows at all durations of ischemic time (1 min, 3 min, 5 min, 10 min). Their minimal vascular resistance (mean blood pressure divided flow) was also higher than controls. This suggests a decreased vasodilator capacity of the forearm musculature and points to a more generalized disorder of smooth muscle function in these patients.